"Dear Steve, I saw a patient this morning with your book [in hand] and highlights throughout. She loves it and finds it very useful to help her in dealing with atrial fibrillation."

Dr. Wilber Su,Cavanaugh Heart Center, Phoenix, AZ

"...masterful. You managed to combine an encyclopedic compilation of information with the simplicity of presentation that enhances the delivery of the information to the reader. This is not an easy thing to do, but you have been very, very successful at it."

Ira David Levin, heart patient, Rome, Italy

"Within the pages of Beat Your A-Fib, Dr. Steve Ryan, PhD, provides a comprehensive guide for persons seeking to find a cure for their Atrial Fibrillation."

dementia

Dementia risk is “strongly associated” with younger patients who develop Atrial Fibrillation. That’s the finding of a 20-year study among 6,196 people without established A-Fib.

Rotterdam Study of Cardiovascular Disease

In a 20-year observational study of participants in the long-term Rotterdam Study, researchers tracked 6,514 dementia-free people. Researchers were monitoring participants for dementia and Atrial Fibrillation. At the start of the study (baseline), 318 participants (4.9%) already had A-Fib.

“The Rotterdam Study” is a long-term study started in 1990 in Rotterdam, The Netherlands. Cardiovascular disease is just one of several targeted diseases.

Results: A-Fib and Dementia

During the course of the study, among 6,196 people without established A-Fib: 11.7% developed A-Fib
and 15.0% developed incident dementia. Other findings:

• Development of A-Fib was associated with an increased risk of dementia in younger people (<67 years old)

• Dementia risk was strongly associated with younger people (<67 years old) who developed A-Fib

• Dementia risk was notstrongly associated in the elder participants who developed A-Fib.

The Rotterdam researchers didn’t state explicitly that A-Fib “causes” dementia. Instead they concluded that A-Fib was “strongly associated” with dementia. Because there may be other factors at play, that’s as far as researchers can go (though they did use regression models to adjust for age, sex, and cardiovascular risk factors).

The younger you are when you develop A-Fib, the more important it is to seek your A-Fib cure to reduce the associated risk of developing dementia.

A-Fib Leads to or Causes Dementia

As patients we have to conclude that, all things being equal, A-Fib leads to and/or causes Dementia. This makes intuitive sense, doesn’t it?

In A-Fib we lose 15%-30% of our heart’s ability to pump blood to our brain, and to the rest of our body. Research confirms that older adults with dementia had significantly reduced blood flow into the brain compared with older adults with normal brain function or young adults.

What Patients Need To Know

The bottom line, the younger you are when you develop A-Fib and/or the longer you have A-Fib, the greater your risk of developing dementia. Seek your A-Fib cure sooner rather than later.

To decrease your increased risk of dementia, your goal should be to get your A-Fib fixed and get your heart beating normally again. We can’t say it enough:

It’s commonly assumed that both sugar–sweetened and artificially-sweetened soft drinks have been linked to cardiometabolic risk factors, which increase the risk of cerebrovascular disease and dementia.

Researchers studied 2,888 participants over 45 years old for incidents of stroke, and 1484 participants over 60 years old for incidents of dementia. Adjustments were made for age, sex, education (for analysis of dementia), caloric intake, diet quality, physical activity, and smoking.

Strategies for Preventing Dementia

What doesn’t work: current drugs, even statins, don’t work or have mixed results in preventing dementia.

What does work: Catheter ablation to eliminate your Atrial Fibrillation. Patients who get a catheter ablation have long-term rates of dementia similar to people without A-Fib. (This result holds regardless of their initial CHADS2 score.)

Americans Rank Alzheimer’s as Most Feared Disease, According to New Marist Poll for Home Instead Senior Care; November 13, 2012 http://www.businesswire.com/news/home/20121113005422/en/Americans-Rank-Alzheimer%E2%80%99s-Feared-Disease-Marist-Poll

“The Rotterdam Study” is a long-term study started in 1990 in Rotterdam, The Netherlands. Cardiovascular disease is just one of several targeted diseases. Since 2008 it has 14,926 participants.

At the start of the study (baseline), 318 participants (4.9%) already had A-Fib.

Results

During the course of the 20-year study, among 6,196 people without established A-Fib:

• 723 participants (11.7%) developed A-Fib, and
• 932 participants (15.0%) developed incident dementia.
• Development of A-Fib was associated with an increased risk of dementia in younger people (<67 years old).
• Dementia risk was strongly associated with younger people (<67 years old) who developed A-Fib but notstrongly associated in the elder participants who developed A-Fib.

Long-term exposure to warfarin and aspirin, if not well controlled, may result in micro bleeds in the brain that accumulate over time raising the risk of dementia, according to Dr. T Jared Bunch of the Intermountain Medical Center, Murray, UT.

Research Findings: Taking Both Warfarin and Aspirin

Speaking at the American Heart Association’s Scientific Sessions 2014, Dr. Bunch described recent research findings on the incidence of dementia in A-Fib patients taking both warfarin (anticoagulant) and aspirin (antiplatelet).

For 10 years, investigators followed 1,031 A-Fib patients with no previous history of stroke or dementia who were taking both warfarin and aspirin (or clopidogrel).

• 25% or more of the time, were more than twice as likely to develop dementia (5.8%).

• 10% –24% of the time, had an incidence of dementia of 4.1%.

• less than 10% of the time had a risk of dementia of 2.7%.

For A-Fib patients taking both warfarin and aspirin, frequent abnormally slow clotting times (an INR score above 3) had a cumulative effect making them more prone to developing dementia.

Previous Research on Warfarin and Dementia

Earlier research found that patients taking warfarin were more likely to develop dementia if their clotting times frequently were too slow or too fast (i.e., an INR above 3 or below 2).

For these A-Fib patients, over-anticoagulation and under-anticoagulation lead to cerebral microbleeds and clots in the brain, important in the development of dementia.

Dr. John Day, a colleague of Dr. Bunch, describes the tragic case of one of his patients who was on warfarin for 10 years and developed cerebral microbleeds and dementia. Read the article.

What The Research Means to A-Fib Patients

According to Dr. Bunch, with warfarin, “it’s very common to have INR outside the ideal range up to 40% of the time, and over the years there may be an accumulative negative impact on cognitive ability.”

Both studies found A-Fib patients on warfarin to be at greater risk of developing dementia. The more recent study found the risk of dementia was greater when taking both warfarin and aspirin, than the risk of dementia when taking warfarin alone.

If you have to take warfarin, don’t start taking aspirin on your own (because you’ve read it’s good for your heart or may reduce cancer risk.) You may be raising your risk of developing dementia.

On Warfarin? How to Reduce the Risk of Dementia

If you are on warfarin because of A-Fib and also have to take aspirin (or clopidogrel) for example because you have a stent, you could be more than twice as likely to develop dementia.

In this case, you probably can’t stop taking aspirin, but there are ways to no longer have to take warfarin.

• You can have your Left Atrial Appendage (LAA) closed off or removed by devices like the Watchman, Lariat II, or surgery with the AtriClip. (Note: 90%-95% of A-Fib clots come from the LAA).

• Consider switching from warfarin to one of the newer anticoagulants such as Eliquis; (But the NOACs are so new, and since they also work by causing bleeding, this strategy may not work. We don’t know if over time they will or will not have similar effects as warfarin.)

Bottom Line: Do Not Routinely Take Both Warfarin and Aspirin

You can no longer afford to routinely take both warfarin (anticoagulant) and aspirin (antiplatelet)! Talk with your doctor about your increased risk of dementia. (Perhaps take along a copy of this post.)

Don’t make changes on your own: Suddenly stopping daily aspirin therapy could have a rebound effect that may trigger a blood clot. If you have been taking daily aspirin therapy and want to stop, it’s important to talk to your doctor before making any changes.

Dr. John Day of the Intermountain Heart Institute, discussed how A-Fib doubles the risk of having a silent stroke. Many studies have shown that A-Fib is independently associated with dementia. “AF is associated with a higher risk for cognitive impairment and dementia, with or without a history of clinical stroke.”

In one study of 11,723 patients, those with arrhythmia were 4½ times more at risk of developing dementia.

Dr. Day described four possible mechanisms that may lead to A-Fib dementia:

Dr. Josef Kautzner’s presentation demonstrated that living with “AF is more dangerous than its ablation” because of the risks of cerebral lesions and cognitive impairment. Small cerebral lesions don’t seem to cause symptoms, but obviously doctors want to avoid creating any kind of lesions on the brain if at all possible.

In MRI tests, a high proportion of A-Fib patients before ablation had silent cerebral infarctions or lesions (60%-80%). But the problem is that similar lesions were detected by MRI even in patients without documented A-Fib.

Therefore, we still do not know how much A-Fib contributes to the development of such lesions. On the other hand, their presence may explain (at least in part) the association between A-Fib and dementia.

Dr. Kautzner’s agenda included demonstrating that living with “AF is more dangerous than its ablation.”

Silent Brain Lesions after Ablation?

Recent studies of mesh-type multielectrode catheters (not yet FDA-approved for use in the US) using MRIs of the brain have revealed silent cerebral ischemia—small lesions on the brain that don’t seem to produce any symptoms and tend to disappear over time. Worldwide experience suggests that small and medium lesions (less than 10mm) disappear at follow-up, while larger than 10 mm lesions remain. These larger lesions make up only a small proportion of the silent lesions found.

Dr. Kautzner pointed out that these silent lesions are common in many interventional procedures such as carotid artery stenting (37%) and TAVI (replacing the Aortic Valve) (68%-77%).

Though these small cerebral lesions don’t seem to cause symptoms, obviously doctors want to avoid creating any kind of lesions on the brain if at all possible.

Cognitive Dysfunction after Ablation?

…by 90 days the POCD rates had dropped down to 13% of paroxysmal and 20% of persistent.

In one study of “Post-Operative Cognitive Dysfunction (POCD)”, two days after standard ablations, about 25% of both paroxysmal and persistent patients experienced POCD, but by 90 days the POCD rates had dropped down to 13% of paroxysmal and 20% of persistent. No MRIs were done of these patients. (If this study had followed these patients for more than three months, the POCD rates for paroxysmal might well have dropped back down to near zero.)

Persistent patients had linear ablation lines added and ablation of complex fractionated electrograms (CFAEs). They also underwent more cardioversions during the procedure than paroxysmal patients. 1

Silent Brain Lesions Before Ablation of Greater Concern

Of greater concern are the silent brain lesions which occur frequently before ablation. In MRI tests, a high proportion of A-Fib patients before ablation had silent cerebral infarctions or lesions (60%-80%). But the problem is that similar lesions were detected by MRI even in patients without documented A-Fib. Therefore, we still do not know how much A-Fib contributes to the development of such lesions. On the other hand, their presence may explain (at least in part) the association between A-Fib and dementia.

We still do not know how much A-Fib contributes to the development of such lesions but their presence may explain the association between A-Fib and dementia.

In one study 89% of paroxysmal and 92% of persistent A-Fib patients had at least one area of SCI (Silent Cerebral Ischemia). The number of SCI areas was higher in patients with persistent A-Fib. These silent brain lesions are associated with dementia. 2

Cognitive performance was significantly worse in patients with paroxysmal and persistent A-Fib than in controls in sinus rhythm. 3

How Silent Brain Lesions Develop During an Ablation

Dr. Kautzner described how these lesions might develop:

• Thrombi due to activation of the coagulation cascade after introduction of catheters. That’s why heparin and other anticoagulants are used before, during and after an RF ablation
• Particulate emboli (char)—making RF burns can potentially produce charring where small particles of heart tissue can break off and travel to the brain. This can be prevented by catheter cooling (irrigated-tip catheters) and prevention of tissue overheating
• Gaseous emboli (micro-bubbles) produced by air on sheaths/catheters or by heating/boiling of blood and heart tissue “steam pops.” Prevention—as above

Preventing Silent Brain Lesions During an Ablation

Dr. Kautzner described the procedures his center follows to prevent silent brain lesions:

• If CHA2DS2-VASc score of 0-1, no prior anticoagulation
• All others have uninterrupted warfarin (persistent have TEE before ablation)
• Aggressive heparinization from the beginning of the procedure, immediately after venous puncture
• Use of intracardiac echocardiography to monitor the procedure

The success of these strategies was documented in a study where DW-MRI and protein S100B testing were performed both before and the next day after the ablation. (DW stands for Diffusion Weighted Imaging MRI which is more sensitive in detecting small & early infarcts [lesions or tissue deaths]).

S100B testing checks the blood for calcium-binding proteins coming from the brain after a stroke. They predict post-ablation brain injury.

S100B testing checks the blood for calcium-binding proteins coming from the brain after a stroke. They predict post-ablation brain injury. In the example from Dr. Kautzner’s center, 1.7% of ablation patients had a new MRI lesion, while 5% had an increase of plasma S100B. (Plasma S100B testing seems to reveal more potential brain damage than an MRI and is certainly easier and cheaper to perform.)

• Persistent A-Fib
• Procedure duration
• Cumulative dose of heparin (ACT—Activated Clotting Time)
• Cardioversion during the procedure
• Age
• CHA2DS2-VASC score
• Amount of RF burns. Patients who had a simple PVI ablation had fewer silent lesions than if linear lesions had to be made. If ablation for CFAEs had to be made, they had even more chance of silent lesions
• Single vs two transseptal punctures

Proposed Strategies to Minimize Risk of Silent Lesions

• Avoid interruption of anticoagulation before ablation
• Use TEE or ICE to detect any thrombus
• Systemic heparin from the beginning of the procedure
• Meticulous management of transseptal sheaths and catheters (including submersion of sheath assembly when loading with special catheters to avoid air bubbles on the sheaths)
• If using phased mesh RF catheters, avoid simultaneous activation of overlapping electrodes
• Consider avoidance of cardioversion during the ablation

Dr. Kautzner’s Conclusions

• Post-ablation asymptomatic cerebral microembolism can be detected with variable frequency
• Clinical consequences are unclear—some studies suggest possible cognitive decline
• On the other hand, there is much stronger evidence that atrial fibrillation is associated with a substantial risk of asymptomatic cerebral lesions and cognitive impairment
• Assessment of procedure-related brain damage (using DW-MRI or protein S100B) should become a standard for the monitoring of safety of novel technologies for ablation

Editor’s Comments:

A-Fib More Dangerous to Cognitive Ability than its Ablation: We are most grateful to Dr. Kautzner for his comprehensive study of A-Fib silent brain lesions. The bottom line is that there is inconclusive evidence that ablations produce lasting linear brain lesions and cognitive decline.

On the other hand, we know from many studies that A-Fib (before ablation) produces silent brain lesions in nearly 90% of cases and that these silent lesions are associated with dementia. Cognitive performance is significantly worse in people with A-Fib (both paroxysmal and persistent). As Dr. Kautzner says, “A-Fib is more dangerous than its ablation,” with regards to silent brain lesions and cognitive ability.

Importance and Frequency of Silent Brain Lesions: I, and I think most of the attendees, were surprised at how prevalent silent cerebral lesions were in patients with A-Fib, and how A-Fib patients have significantly worse cognitive performance. This is yet another reason not to leave patients in A-Fib, and for those of us with A-Fib to get treatment and/or an ablation as reasonably soon as possible.

S100B testing seems a great way to test for brain damage

S100B Testing: S100B testing seems a great way to test for brain damage after an ablation. Most centers (and insurance companies in the US) won’t routinely do an MRI after an ablation. But an S100B plasma test is more easily and cheaply performed, and may be more accurate than an MRI. But then the question for doctors and patients is what should be done if a S100B test comes out positive? If there are no brain damage symptoms, how concerned should we be?

FAQs: Mineral Deficiencies & Supplements for a Healthy Heart

A-Fib patients often look for non-drug approaches to ease or prevent the symptoms of their Atrial Fibrillation. Here we share answers to the most often asked questions about minerals deficiencies and the use of supplements.

2. How can I tell if I’m lacking in Vitamin D? I’m concerned because Vitamin D deficiency has been tied to both A-Fib and Dementia. What is a normal level of Vitamin D?

Vitamin D is important in virtually every tissue and cell in your body. Low blood levels of vitamin D have been associated with increased risk of death from cardiovascular disease, cognitive impairment in older adults and cancer.

The production of vitamin D from the skin decreases with age. In addition, people who have darker skin need more sun exposure to produce adequate amounts of vitamin D, especially during the winter months. Keep in mind that your Vitamin D level in the summer when you get more sun and UVB is probably higher than in the winter.

Testing Options Ask your doctor for a “25-hydroxy Vitamin D Test”. (There is another type of blood test for vitamin D, called a 1,25(OH)₂D test, but the 25(OH)D test is the only one that will tell you whether you’re getting enough vitamin D.)

What Is an Optimal 25(OH)D Level? Vitamin D deficiency is defined as a blood 25(OH)D level below 20 ng/dL. Normal levels are considered to be above 30 ng/dL. (Some sources consider that ‘optimal’ levels are between 50ng/dL–70ng/dL .)

Sun Exposure and Supplements If you tested low, you need to get more sun exposure and/or take a daily supplement (Vitamin D supplementation is safe and inexpensive). For supplement dosage, see Treatments/Mineral Deficiencies.

Monitoring A blood test is recommended to monitor blood levels of 25(OH)D three months after beginning treatment. The dose of vitamin D may need to be adjusted based on these results.

1. “I’m scared of getting dementia. Can the right minerals help? I’ve read about the link with A-Fib. What does research reveal about this risk?”

A-Fib and Dementia are two diseases that seem to parallel each other. Like A-Fib, Dementia seems to increase with age, diabetes, hypertension, heart failure, smoking history, and systemic inflammation. Dr. T. Jared Bunch of the Intermountain Medical Center in Utah, identified two other mechanisms of both A-Fib and Dementia: Vitamin D Deficiency and the APOE gene. Both cause less blood to the brain and loss of oxygen, mini clots and vascular problems.

Ablation Decreases Risk of Dementia and Risk of Stroke and Early Death

Several studies showed that people with A-Fib who had an ablation had about the same risk of Dementia (and the same risk of having a stroke) as normal people, while people with A-Fib who didn’t have an ablation had much more risk of developing Dementia (and higher 5 year stroke risk). [Ablation probably increases blood flow to the brain and is responsible for decreasing the risk of Dementia.]

• Vitamins B6, B12, Folate, and Vitamin D Vitamin D deficiency tracks with the development of both Dementia and A-Fib, but it’s not yet known if supplementation reduces the risk.

• Omega Fatty Acids/Fish Oil Low intake is associated with Dementia; studies do show the benefit of fish consumption on the risk of Dementia and cognitive decline.

Active Lifestyle

Patients with more active lifestyles have lower risks of Dementia and cognitive decline.

What this means to you: Early intervention, such as A-Fib ablation, proper vitamins and minerals, along with an active lifestyle may improve long-term cognitive outcomes and reduce the risk of Dementia to that of patients with no history of A-Fib.

A-Fib-Free After Catheter Ablation, Patient on Anticoagulation Therapy for 10 years Develops Cerebral Microbleeds and Associated Early Dementia.

By Steve S. Ryan, Updated March 2016

Dr. John Day, in an editorial in The Journal of Innovations in Cardiac Rhythm Management, described his patient, Bob, who had been on anticoagulation therapy for 10 years, even though he had had a successful catheter ablation and was A-Fib free.

Of concern, these new guidelines call for many more people to be on anticoagulant therapy, particularly women.

Bob was suffering from early dementia. A cranial MRI revealed many cerebral microbleeds, probably caused by taking anticoagulants for years. Both antiplatelet and anticoagulant therapy significantly increase the risk of cerebral microbleeds which are associated with dementia. These microbleeds are usually permanent and irreversible.

Dr. Day asked, “Could it be that this was an iatrogenic (caused by a doctor’s activity or therapy) case of dementia? Was his 10 years of anticoagulant use for atrial fibrillation the cause of his dementia?”

The 2014 CHA2DS2-VASc Guidelines for Anticoagulation Therapy

Dr. Day discusses the new CHA2DS2-VASc guidelines for anticoagulation therapy. He points out that none of the major studies supporting the CHA2DS2-VASc guidelines have reported the accompanying cerebral microbleed risk. He also calls our attention to the reports from many centers that long-term stroke risk following catheter ablation is very low. Ablation may reduce the total arrhythmia burden or convert recurrences to more organized rhythms, such as an atrial tachycardia, with a lower stroke risk.

This effect of A-Fib ablation isn’t recognized in the latest guidelines.

So, the question is, ‘Why the risks of life-long anticoagulation therapy if the patient has had a successful ablation procedure?’

Also, these new guidelines call for many more people to be on anticoagulant therapy, particularly women. Dr. Day does not go so far as to say the new guidelines are in error (as I do), but he does ask,” What about the 35 year old woman with borderline hypertension and only one A-Fib recurrence each year? Should she now take anticoagulants for the rest of her life even if she has had a successful ablation?”

(See more research contradicting the 2014 Guides: A study using the Taiwan Research Database of 186,570 A-Fib patients, they discounted female gender and only looked at females with a CHA2DS2-VASc score of 2 (one additional risk factor besides being female).1,2,3

Warning: The Risks of Life-long Anticoagulation Therapy

Dr. Day concludes, “Somehow I think we have lost sight of the total picture with the new A-Fib management guidelines. In my mind, I am not convinced that the long-term stroke risk of a CHA2DS2-VASc score of 1 or 2 (depending on which risk factors are present) justifies all of the risks of life-long anticoagulation therapy, particularly if the patient has had a successful ablation procedure.”4 Dr. John Mandrola echoes Dr. Day, “And if there is no A-Fib, there is no benefit from anticoagulation.”5 Anticoagulants are not like taking vitamins, “Oral anticoagulants are high-risk medications.”6

Editorial comments:

“But CHA2D2-VASc are just guidelines, aren’t they? Doctors don’t have to follow them, do they?”

Unfortunately once guidelines like these become official, they in effect become the law of the land. If a doctor doesn’t follow them and a patient has a stroke, the doctor is almost guaranteed a losing malpractice law suit. The first thing a trial lawyer will point out to an arbitrator or jury is that the doctor didn’t follow current guidelines.

This puts doctors in a very difficult position. Even though Dr. Day knows all too well and agonizes over the fact that his anticoagulant therapy probably caused his patient Bob’s dementia, he can’t change the guidelines.

Disclaimer: the authors of this Web site are not medical doctors and are not affiliated with any medical school or organization. The information on this site is not intended nor implied to be a substitute for professional medical advice. Always seek the advice of your physician or other qualified health professional prior to starting any new treatment or with any questions you may have regarding a medical condition. Nothing contained in this service is intended to be for medical diagnosis or treatment.